title: Platelet lysate induces in vitro wound healing of human keratinocytes associated with a strong proinflammatory response.
abstract: Platelet lysates (PL), which are derived from platelets, are cocktails of growth factors and cytokines that can promote tissue regeneration. Until today, most studies have focused on growth factor content of platelets rather than on their potential as a reservoir of mediators and cytokines. Taking advantage of an in vitro scratch assay performed under both normal and inflammatory conditions, in the present work, we report that at physiologic concentrations, PL enhanced wound closure rates of NCTC 2544 human keratinocytes. This effect was clearly detectable 6 h after wounding. Moreover, PL induced a strong cell actin cytoskeletal re-organization that persisted up to 24 h. The accelerated wound closure promoted by PL, in either presence or absence of serum, was associated with a high expression of the inflammatory cytokine interleukin-8. Further, after 24 h PL treatment, confluent keratinocytes also expressed low amounts of interleukin-8 and of the antimicrobial peptide neutrophil gelatinase-associated lipocalin, which dramatically increased under inflammatory conditions. These effects were associated with activation of the inflammatory pathways, p38 mitogen-activated protein kinase, and NF-κB. Our findings support the concept that platelet-derived preparations could accelerate regeneration of difficult-to-heal wounds by triggering an inflammatory cascade and having an antimicrobial role.
authors.affiliation: Dipartimento di Oncologia, Biologia e Genetica, Universita'di Genova, Genova, Italy.
authors.forename: Rania
authors.initials: R
authors.lastname: El Backly
authors.forename: Valentina
authors.initials: V
authors.lastname: Ulivi
authors.forename: Laura
authors.initials: L
authors.lastname: Tonachini
authors.forename: Ranieri
authors.initials: R
authors.lastname: Cancedda
authors.forename: Fiorella
authors.initials: F
authors.lastname: Descalzi
authors.forename: Maddalena
authors.initials: M
authors.lastname: Mastrogiacomo
mesh_terms: D000199:Actins / Q000378:metabolism; D000209:Acute-Phase Proteins / Q000378:metabolism; D000890:Anti-Infective Agents / Q000494:pharmacology; D001792:Blood Platelets / Q000187:drug effects / Q000378:metabolism*; D002457:Cell Extracts / Q000494:pharmacology*; D002460:Cell Line; D002465:Cell Movement / Q000187:drug effects; D048430:Cell Shape / Q000187:drug effects; D003599:Cytoskeleton / Q000187:drug effects / Q000378:metabolism; D004789:Enzyme Activation / Q000187:drug effects; D006801:Humans; D007249:Inflammation / Q000473:pathology*; D016209:Interleukin-8 / Q000378:metabolism; D007501:Iron / Q000378:metabolism; D015603:Keratinocytes / Q000187:drug effects* / Q000201:enzymology / Q000473:pathology*; D000071068:Lipocalin-2; D054834:Lipocalins / Q000378:metabolism; D016328:NF-kappa B / Q000378:metabolism; D011518:Proto-Oncogene Proteins / Q000378:metabolism; D014945:Wound Healing / Q000187:drug effects*; D048051:p38 Mitogen-Activated Protein Kinases / Q000378:metabolism
chemical_list: D000199:Actins; D000209:Acute-Phase Proteins; D000890:Anti-Infective Agents; D002457:Cell Extracts; D016209:Interleukin-8; C489506:LCN2 protein, human; D000071068:Lipocalin-2; D054834:Lipocalins; D016328:NF-kappa B; D011518:Proto-Oncogene Proteins; D007501:Iron; D048051:p38 Mitogen-Activated Protein Kinases